LP is very uncommon in children and occurs most often in adults in their fourth, fifth, and sixth decades. Family clusters are occasionally seen. Most cases begin insidiously with the onset of intensely pruritic red to deeply violet-colored papules that gradually increase in number and extent until the patient is sufficiently symptomatic to seek relief. A small number of cases present with a dramatic generalized exanthematic onset. These patients are immensely uncomfortable and socially devastated. Occasionally, painful oral lesions predominate. Uncommon nail, follicular, and ulcerating variants will not be discussed in this chapter.
A small number of cases will resolve spontaneously within a few weeks. Ninety percent of cases will resolve by 24 months. About 10% of patients will develop chronic LP, usually in the form of oral mucous membrane lesions or hypertrophic lesions on the lower limbs. Occasionally, patients present with recurrent episodes that are separated by symptom-free periods. Some patients have only a small number of lesions in a very limited area, while others have hundreds of lesions over much of the body surface. Almost all complain of intense itch that is disproportionate to the visible rash.
LP begins with tiny papules that retain the skin marking lines and are therefore geometric or polygonal in shape. When first seen they are usually 3 to 5 mm in size and are palpably raised. Individual lesions can enlarge up to 1 cm. When lesions are grouped, they can merge to form tight aggregates of considerable size. They may then evolve into plaques or their papular origin may remain evident.
Some cases of LP are precipitated by a chronic tinea pedis and will resolve and recur with the activity of the fungal infection. Like psoriasis, LP will activate at sites of trauma and therefore shows a true Koebner phenomenon. In this disease, however, trauma induction is an incidental sign that supports the diagnosis but does not contribute in any significant way to the extent of the disease. A wide range of medications produce LP-like drug eruptions; however, it is uncertain at present whether these represent a separate entity or unmasking of idiopathic LP.
Self-treatment is not a problem in LP, except where a covert medication might cause an LP-like drug eruption.
A careful medication history is essential, and any medication reported to cause an LP-like eruption should be discontinued. The features of these drug eruptions are sometimes strikingly similar to the idiopathic disease both clinically and microscopically, and offending drugs will be uncovered only by careful history. The list of medications that cause these reactions continues to grow and any agent should be suspect. These drug-induced eruptions are slow to clear and it is not unusual for improvement to take 2 or 3 months. LP has also been associated with an increased incidence of autoimmune diseases (Sjogren's syndrome, sicca syndrome, alopecia areata, vitiligo, ulcerative colitis, myasthenia gravis, and diabetes mellitus), chronic dermatophyte infections, and chronic liver disease (primary biliary cirrhosis, alcoholic cirrhosis, chronic active hepatitis B and C). The presence of a fungal infection is usually significant: the authors have seen many cases of LP that clear and exacerbate with its activity. LP-like lesions are seen in patients with graft-versus-host reactions.
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